ReviewJournal of virology2020
The Dynamic Interface of Viruses with STATs.
Review in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed.
- Integration of a multimeric STAT consensus site into the adenoviral genome to interfere with IFN signaling represents a novel concept to improve oncolytic virotherapy.Journal of virology · 2026Article
- Single-cell transcriptomic analysis deciphers heterogeneity and transcriptional regulatory programs of sepsis with different prognosis.Biology direct · 2026Article
- Hendra virus genotypes 1 and 2 differ in V protein-mediated immune evasion.The Journal of general virology · 2026Article
- HIV-1 Nef inhibits the JAK/STAT signaling pathway by inducing proteasomal degradation of STAT1.PloS one · 2026Article
- Article
- Solution structure of the C-terminal domain of the measles virus V protein in its free form and mechanistic analysis of STAT2 targeting.Journal of virology · 2025Article
- Sec10 suppresses antiviral innate immune response by facilitating STUB1-mediated STAT1 degradation.PLoS pathogens · 2025Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Article
- Investigating how dengue virus-induced metabolic changes affect the host immune response and how to develop Immunomodulatory strategies.Virology journal · 2025Review
- The segmented flavivirus Alongshan virus reduces mitochondrial mass by degrading STAT2 to suppress the innate immune response.Journal of virology · 2025Article
- Review
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Exploring JC Polyomavirus Sequences and Human Gene Expression in Brain Tissue of Patients With Progressive Multifocal Leukoencephalopathy.The Journal of infectious diseases · 2024Article
- Suppression of the host antiviral response by non-infectious varicella zoster virus extracellular vesicles.Journal of virology · 2024Article
- A Bayesian noisy logic model for inference of transcription factor activity from single cell and bulk transcriptomic data.NAR genomics and bioinformatics · 2023Article
- Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host.Virologica Sinica · 2023Article
- Unveiling the immunomodulatory shift: Epithelial-mesenchymal transition Alters immune mechanisms of amniotic epithelial cells.iScience · 2023Article
- An aquatic virus exploits the IL6-STAT3-HSP90 signaling axis to promote viral entry.PLoS pathogens · 2023Article
- Targeting Human Proteins for Antiviral Drug Discovery and Repurposing Efforts: A Focus on Protein Kinases.Viruses · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses commonly antagonize the antiviral type I interferon response by targeting signal transducer and activator of transcription 1 (STAT1) and STAT2, key mediators of interferon signaling. Other STAT family members mediate signaling by diverse cytokines important to infection, but their relationship with viruses is more complex. Importantly, virus-STAT interaction can be antagonistic or stimulatory depending on diverse viral and cellular factors. While STAT antagonism can suppress immune pathways, many viruses promote activation of specific STATs to support viral gene expression and/or produce cellular conditions conducive to infection. It is also becoming increasingly clear that viruses can hijack noncanonical STAT functions to benefit infection. For a number of viruses, STAT function is dynamically modulated through infection as requirements for replication change. Given the critical role of STATs in infection by diverse viruses, the virus-STAT interface is an attractive target for the development of antivirals and live-attenuated viral vaccines. Here, we review current understanding of the complex and dynamic virus-STAT interface and discuss how this relationship might be harnessed for medical applications.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.